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From:
Jennie Brand Miller <[log in to unmask]>
Reply To:
Paleolithic Diet Symposium List <[log in to unmask]>
Date:
Mon, 11 May 1998 10:54:48 +1100
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Thanks Art for your comments.  I'm so pleased to hear someone agrees with
me in this era of the thrifty genotype.

On the suject of fat, deposition, I have a hunch that it is the COMBINATION
of high fat and high GI carbohdyrate that triggers weight gain.  When we
eat this type of meal (which is most of the time), the insulin stimulated
by the high GI carbohdyrate (mainly wheat flour and potatoes by the way,
not sugar), the body's response is to switch off lipolysis in the adipose
tissue stores (this is one of the most important functions of insulin) so
that free fatty acids are no longer secreted into the bloodstream.  Glucose
becomes the main source of fuel when insulin is high.  This means that the
fat in the meal needs to be 'tucked away' somewhere to await oxidation when
insulin levels decline.  We all know where it gets tucked away. What's
more, the adipose tissue is staying put while ever insulin levels remain
high.

Because insulin resistant individuals have an extremely pronounced insulin
response to CHO feeding (especially high GI CHO), insulin levels remain
high for longer and free fatty acids remain unoxidised for longer.  Over
the course of years this imbalance in CHO/fat oxidation lends itself to a
steady accumulation of body fat.

I think very high CHO, low fat diets 'work' (in limiting weight gain)
partly because they are generally bulky, satiating and hard to ingest in
excess, but partly because they mean that there is less fat to be 'tucked
away', for burning later on.

We have rat experiments in progress at the moment to test this hypothesis.

Best wishes  Jennie


Jennie Brand Miller  PhD
Associate Professor in Human Nutrition
Department of Biochemistry  G08
University of Sydney
NSW 2006  Australia
Phone: (61 2) 9351 3759
Fax: (61 2) 9351 6022

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